926 Myocardial Infarction
• Type 4a: MI associated with percutaneous
BASIC INFORMATION
DEFINITION
Myocardial infarction (MI) is a clinical syn-
drome characterized by symptoms of myocar-
dial ischemia, persistent electrocardiographic
(ECG) changes, and release of biomarkers of
myocardial necrosis resulting from an insuf-
ficient supply of oxygenated blood to an area
of the heart. According to the European Society
of Cardiology/American College of Cardiology
guidelines, the following criteria for acute evolv-
ing or recent MI satisfies the diagnosis:
1. Detection of the rise and/or fall of cardiac bio-
marker values (preferably cTn) with at least 1
value above the 99th percentile and with at
least 1 of the following:
• Symptoms of ischemia
• New, or presumed new, significant ST-T
changes or new LBBB
• New ST elevation at the J point in at least 2
contiguous leads of ≥2 mm (0.2 mV) in men
or ≥1.5 mm (0.15 mV) in women in leads
V2–V3 and/or of ≥1 mm (0.1 mV) in other
contiguous chest leads or the limb leads
• Development of pathologic Q waves in the
ECG
2. Imaging evidence of new loss of viable myo-
cardium or a new regional wall motion abnor-
mality
3. Identification of an intracoronary thrombus by
angiography or autopsy pathologic findings of
acute MI
MI may be classified as ST-segment eleva-
tion MI (STEMI) and non–ST-segment elevation
MI (NSTEMI) depending on the ECG findings on
MI presentation. This entry primarily focuses on
STEMI. For a discussion of NSTEMI, see “Acute
Coronary Syndromes.”
There are five subtypes of acute MI:
• Type 1: Spontaneous MI related to ischemia
due to a primary coronary event such as
plaque erosion and/or rupture, fissuring, or
dissection.
•  Type 2: MI secondary to ischemia, other
than coronary artery disease, due to either
increased oxygen demand or decreased sup-
ply (e.g., coronary endothelial dysfunction,
coronary artery spasm, coronary embolism,
anemia, arrhythmias, respiratory failure,
hypertension with/without LVH, or hypoten-
sion). Also in critically ill patients or in
patients undergoing major noncardiac sur-
gery, elevated values of cardiac biomarkers
may appear due to the direct toxic effects of
endogenous or exogenous high circulating
catecholamine levels.
• Type 3: Sudden unexpected cardiac death,
including cardiac arrest, often with symp-
toms suggestive of myocardial ischemia,
accompanied by presumed new ST elevation,
new left bundle branch block, or evidence of
fresh thrombus in a coronary artery by angi-
ography and/or at autopsy, or death occurring
before blood samples could be obtained or
at a time before the appearance of cardiac
biomarkers in the blood.
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EPIDEMIOLOGY &
coronary intervention. Elevation of cTN >5×
percentile of upper reference limit (URL) in
patients with normal baseline value, or a rise
of cTN >20% if the baseline values are stable
and are stable or falling. In addition to either
symptoms of ischemia, new ischemic ECG
changes or new LBBB, or angiographic loss
of a patent coronary artery, persistent slow or
no-flow, or embolization, or imaging of new
wall motion abnormality.
• Type 4b: MI associated with stent thrombosis
as documented by angiography or at autopsy
in the setting of myocardial ischemia and
with a rise/fall of cardiac biomarker values.
• Type 5: MI associated with coronary artery
bypass grafting. Elevation of cardiac bio-
marker values >10× 99% URL in patients
with normal baseline cTn values, in addition
to either new pathological Q waves or new
LBBB, or new native coronary artery occlu-
sion or imaging of new abnormal wall motion
abnormality.
SYNONYMS
MI
Myocardial infarction
ST-elevation MI
Heart attack
Acute myocardial infarction
AMI
Coronary thrombosis
Coronary occlusion
ICD-10CM CODES
I21.01 ST elevation (STEMI) myocardial
infarction involving left main coronary
artery
I21.02 ST elevation (STEMI) myocardial
infarction involving left anterior
descending coronary artery
I21.09 ST elevation (STEMI) myocardial
infarction involving other coronary
artery of anterior wall
I21.11 ST elevation (STEMI) myocardial in-
farction involving right coronary artery
I21.19 ST elevation (STEMI) myocardial
infarction involving other coronary
artery of inferior wall
I21.21 ST elevation (STEMI) myocardial
infarction involving left circumflex
coronary artery
I21.29 ST elevation (STEMI) myocardial
infarction involving other sites
I21.3 ST elevation (STEMI) myocardial
infarction of unspecified site
I21.4 Non-ST elevation (NSTEMI)
myocardial infarction
I22.0 Subsequent ST elevation (STEMI)
myocardial infarction of anterior wall
I22.1 Subsequent ST elevation (STEMI)
myocardial infarction of inferior wall
I22.2 Subsequent non-ST elevation
(NSTEMI) myocardial infarction
I22.8 Subsequent ST elevation (STEMI)
myocardial infarction of other sites
I22.9 Subsequent ST elevation (STEMI) myo-
cardial infarction of unspecified site
DEMOGRAPHICS
INCIDENCE/PREVALENCE (IN U.S.):
• According to data from National Health and
Nutrition Examination Survey (NHANES) 2009
to 2012 (National Heart, Lung, and Blood
Institute [NHLBI] tabulation), the overall prev-
alence for MI is 2.8% in U.S. adults ≥20 years
of age. MI prevalence is 4.0% for men and
1.8% for women.
• In 2013 in the U.S., coronary heart dis-
ease alone caused ≈1 of every 7 deaths.
In 2013, 370,213 Americans died of coro-
nary heart disease. Each year, an estimated
660,000 Americans have a new coronary
attack (defined as first hospitalized myo-
cardial infarction or coronary heart dis-
ease death), and 305,000 have a recurrent
attack. It is estimated that an additional
160,000 silent myocardial infarctions occur
each year. Approximately every 34 seconds,
one American has a coronary event, and
approximately every 1 minute 24 seconds,
an American will die of one.
• Community incidence rates as well as mor-
tality rates from STEMI have declined over
the past decade, whereas those for NSTEMI
have increased. At present, STEMI comprises
approximately 30% to 40% of MI presen-
tations. In-hospital mortality (approximately
5%-6%) and 1-year mortality (approximately
7%-18%). The most common cause of death in
adults over the age of 40 is myocardial infarc-
tion. A heart attack takes the life of >1,500,000
people each year in the United States.
• Modifiable risk factors such as hyperten-
sion, diabetes, and cigarette smoking have
recently declined, although hyperlipidemia
has shown no significant change, and obesity
has steadily increased.
• Tobacco use remains the second-leading
cause of total deaths and disability. The
percentage of adults who reported current
cigarette use declined from 24.1% in 1998
to 16.9% in 2014. Still, almost one-third of
coronary heart disease deaths are attribut-
able to smoking and exposure to secondhand
smoke. Patients with first acute MI were
found to have an almost threefold increase
in cigarette smoking from 2002 to 2009.
Cigarette smoking is associated with endo-
thelial dysfunction, prothrombotic defects,
and increased oxidative stress.
• It is more prevalent in males between the
ages of 45 and 65 years old; there is no pre-
dominant sex differential after the age of 65.
• Women comprised 30% of STEMI patients.
They experience more lethal and severe first
acute MIs than men regardless of comorbidi-
ty, previous angina, or age. Studies have sug-
gested that women are less likely to receive
reperfusion therapy, have longer reperfusion
times, are often given the standard of care
treatment within 24 hours of presentation,
and have higher risk of bleeding with anti-
thrombotic therapy.
• At least one-fourth of all MIs are clinically
unrecognized. Approximately 23% of patients
 Myocardial Infarction 927

with STEMI in the U.S. have diabetes mel-
litus, and three-quarters of all deaths among
patients with diabetes mellitus are related to
coronary artery disease. Diabetes mellitus is
associated with higher short- and long-term
mortality after STEMI. In the CRUSADE trial,
7% of eligible patients did not receive reper-
fusion therapy. The most important factor for
not providing reperfusion therapy in eligible
patients was increasing age.
PHYSICAL FINDINGS & CLINICAL
PRESENTATION
• Cardiac auscultation may reveal an apical
systolic murmur caused by mitral regurgita-
tion from papillary muscle dysfunction; S3 or
S4 may also be present.
• Up to 10% of patients may present with acute
pulmonary edema and/or cardiogenic shock.
• Physical examination may be completely normal.
ETIOLOGY
• Coronary atherosclerosis and plaque rupture
• Coronary artery spasm
• Coronary embolism (caused by infective
endocarditis, rheumatic heart disease, intra-
DIAGNOSIS M
DIFFERENTIAL DIAGNOSIS
The various causes of myocardial ischemia are
described along with the differential diagnosis
of chest pain.
LABORATORY TESTS
• Electrocardiogram (Fig. 1): a 12-lead ECG
should be performed and shown to an experi-
enced emergency physician within 10 min of

The clinical presentation of myocardial infarc-
tion is usually based on a history of substernal
pressure type chest pain radiated to the neck,
lower jaw, left arm, or mid-back lasting 20
min or more that is not completely relieved
by sublingual nitroglycerin. The pain may not
be severe. Some patients may present with
atypical symptoms such as nausea/vomiting,
shortness of breath, fatigue, palpitations, and
diaphoresis. The elderly in particular may pres-
ent with dizziness, or syncope. The patients
who tend to present with atypical symptoms
are more likely to be women, diabetic patients,
or elderly patients and less frequently receive
reperfusion therapy and other evidence-based
therapies than patients with a typical chest pain
presentation. Records show that up to 30%
of patients with STEMI present with atypical
symptoms.
Physical findings:
• Skin may be diaphoretic and exhibit pallor
(because of decreased oxygen).
• Rales may be present at the bases of lungs
(indicative of heart failure [HF]).
cavitary thrombus, atrial fibrillation)
• Periarteritis and other coronary artery inflam-
matory diseases
• Dissection into coronary arteries (aneurysmal
or iatrogenic)
• Calcium supplementation may promote vascu-
lar calcification. Studies have shown that cal-
cium supplementation (but not dietary calcium
intake) is associated with elevated risk for MI.
• MI with normal coronaries: more frequent in
younger patients and cocaine addicts. The risk of
acute MI is increased by a factor of 24 during the
60 min after the use of cocaine in persons who
are otherwise at relatively low risk. Most patients
with cocaine-related MI are young, nonwhite,
male cigarette smokers without other risk fac-
tors for coronary heart disease and who have a
history of repeated cocaine use. Blood and urine
toxicology screen for cocaine is recommended
in all young patients who present with acute MI.
• Hypercoagulable states, increased blood vis-
cosity (polycythemia vera and autoimmune
diseases such as systemic lupus, antiphos-
pholipid syndrome)
and Disorders
Diseases
ED arrival for all patients with chest discomfort
(or anginal equivalent) or other symptoms
suggestive of STEMI. Table 1 describes ECG
findings in myocardial infarction. If the initial
ECG is not diagnostic for STEMI but the patient
remains symptomatic and there is a high clini-
cal suspicion for STEMI, serial ECGs at 5- to
10-minute intervals or continuous 12-lead
I
ST-segment monitoring should be performed
to detect the potential development of ST
elevation. In patients with inferior STEMI, right-
sided ECG leads should be obtained to look
for ST elevation suggestive of right ventricular
(RV) infarction. The joint ESC/ACCF/AHA com-
mittee for the definition of MI established the
definition for the diagnosis of ST-elevation
MI, which is considered to be present when
there is an ST-segment elevation in two
contiguous leads, ≥2 mm for men and ≥1.5
mm for women in precordial leads and/or ≥1
mm in limb leads. ST-segment elevation is
measured at 0.08 sec after the J point (the
junction between the end of the QRS and the
beginning of the ST segment). In addition, ST

1 2

B C

A A B
D E
C
3
4

B C
A

A B
FIG. 1  Electrocardiographic findings of acute myocardial infarction (AMI). 1, T-wave abnormalities of
AMI. A, Prominent “hyperacute” T wave. B-E, T-wave inversions of non-ST-segment elevation MI (NSTEMI). 2,
ST-segment depression. A, Flat. B, Downsloping. C, Upsloping. 3, ST-segment elevation. A, Convex ST-segment
elevation. B, Obliquely straight ST-segment elevation. C, Convex ST-segment elevation. 4, Pathologic Q waves.
A, Pathologic Q wave of completed myocardial infarction. B, Simultaneous ST-segment elevation with patho-
logic Q wave 2 hours into the course of ST-segment elevation MI (STEMI). (From Vincent JL, et al.: Textbook of
critical care, ed 6, Philadelphia, 2011, Saunders.)

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928 Myocardial Infarction
TABLE 1  Leads Showing
Abnormal Electrocardiographic
Findings in Myocardial Infarction
Limb Precordial
Leads Leads
Lateral I, aVL V5, V6
Anterior V1, V2, V3
Anterolateral I, aVL V2–V6
Diaphragmatic II, III, aVF
Posterior V1–V3*
* None of the leads is oriented toward the posterior surface of
the heart. Therefore, in posterior infarction, changes that
would have been present in the posterior surface leads will
be seen in the anterior leads as a mirror image (e.g., tall and
slightly wide R waves in V1 and V2, comparable to abnormal
Q waves, and tall and wide, symmetric T waves in V1 and V2).
From Park MK: Park’s pediatric cardiology for practitioners, ed
6, Philadelphia, 2014, Elsevier.
depression in >2 precordial leads (V1–V4) may
indicate transmural posterior injury; multilead
ST depression with coexistent ST elevation in
lead aVR has been described in patients with
left main or proximal left anterior descending
artery occlusion.
• New or presumably new LBBB at presenta-
tion occurs infrequently, may interfere with
ST-elevation analysis, and should not be
considered diagnostic of acute myocardial
infarction (MI) in isolation.
• ECG findings alone, without laboratory
results, are sufficient to diagnose STEMI;
therefore, treatment should not be delayed
until biomarkers are available.
• Cardiac troponin levels: Cardiac-specific tro-
ponin T (cTnT) and cardiac-specific troponin
I (cTnI) are generally indicative of myocardial
injury with increases in serum levels of >99th
percentile of a normal reference population.
Detection of a rise and fall pattern of the
measurements is essential to the diagnosis of
AMI. The rise may occur relatively early after
muscle damage (3-6 hr), peak at 12 to 16 hr,
and may be present for several days after MI
(up to 7 days for cTnI and more than 14 days
for cTnT). cTnT or cTnI tests can be falsely
positive for myocardial infarction in patients
with renal failure, heart failure, myocarditis,
aortic dissection, and pulmonary embolism.
Recently, highly sensitive troponin assays (hs-
cTnI, hs-cTnT) have also been developed
to facilitate an early diagnosis of AMI. Most
patients can be diagnosed with AMI within the
first 2 to 3 hours of presentation. However, an
initial negative high-sensitivity troponin at the
time of presentation is not sensitive enough to
completely rule out AMI. MI can be excluded in
most patients by 6 hours of presentation, and
guidelines suggest serial samples be obtained
every 3 to 6 hours after an initial sample if
there is a high degree of suspicion for AMI.
• Troponin is the preferred marker for the diag-
nosis of myocardial necrosis. A single high-
sensitivity assay for cardiac troponin (hs-CTnT)
concentration below the limit of detection in
combination with a nonischemic ECG may suc-
cessfully rule out an MI in patients presenting
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to EDs with possible emergency acute coronary
syndrome.1 Because troponins need 7 to 14
days to be cleared by the kidneys, they are not
sensitive enough to detect a recurrent MI within
days from the initial MI. CK-MB isoenzyme can
be useful in such circumstances.
• CK-MB isoenzyme is also a useful marker for MI
if troponin levels are not available. It is released in
the circulation in amounts that correlate with the
size of the infarct. An increased CK-MB value for
the diagnosis of MI is defined as a measurement
above the 99th percentile of the upper reference
limit. CK-MB can be detected within 3 to 8 hr of
the onset of chest pain, peak at 12 to 24 hr, and
return to baseline levels within 24 to 48 hr.
IMAGING STUDIES
Imaging studies such as a high-quality portable
chest x-ray, transthoracic echocardiography, and
a contrast chest CT scan should be used to dif-
ferentiate STEMI from aortic dissection, pulmo-
nary embolism, and other intrathoracic causes of
chest pain (i.e., pneumonia and pneumothorax)
in patients for whom this distinction is initially
unclear, or to assess for complications of AMI such
as pulmonary edema. Transthoracic echocardiog-
raphy may provide evidence of focal wall motion
abnormalities and facilitate triage in patients with
ECG findings that are difficult to interpret.
RISK ASSESSMENT
Several risk assessment models are available. In
the TIMI risk score for STEMI, the mean 30-day
mortality was 6.7%. It is composed of eight base-
line variables. The risk score showed a >40-fold
graded increase in mortality, with scores ranging
from 0 to >8 (P <0.0001); 30-day mortality was
0.1% among patients with a score of 0, 2.25 with
a score of 5, and >8.8% among patients with a
score of 8 or greater. The variables are divided
between historical, exam, and presentation:
Historical:
1. Age 65 to 74 (2 points), >75 (3 points),
2. Diabetes/HTN or angina (1 point).
Exam:
1. SBP <100 mm Hg (3 points),
2. Heart rate >100 bpm (2 points),
3. Killip 2 to 4 (2 points),
4. Weight <67 kg (1 point).
Presentation:
1. Anterior ST elevation or LBBB (1 point),
2. Time to reperfusion >4 hr (1 point).
The higher the score, the higher the 30-day
mortality rate. Risk assessment is a continuous
process that should be repeated throughout
hospitalization and at time of discharge.
TREATMENT
NONPHARMACOLOGIC THERAPY
• Limit patient’s activity: bed rest with bedside
commode for the initial 12 to 24 hr. If the patient
remains stable, gradually increase y.1
1 Pickering
JW, et al.: Rapid rule-out of acute myocardial
infarction with a single high-sensitivity cardiac troponin
T measurement below the limit of detection: a collabora-
tive meta-analysis, Ann Intern Med 166:715-724, 2017.
• Diet: nothing by mouth until stable, then clear
liquids as tolerated to advance gradually to
a diet tailored to the patient’s comorbidities
(i.e., diabetes, hypertension, heart failure,
hyperlipidemia, renal failure, COPD, etc.).
• Patient education to decrease the risk of sub-
sequent cardiac events, counseling on smoking
cessation, dietary restrictions, regular exercise,
and medication compliance should be initiated
when the patient is medically stable.
ACUTE GENERAL Rx
• Fig. 2 shows a treatment algorithm for STEMI.
Assessment and treatment algorithm for non-
ST-segment MI is described in Fig. 3. Rationale
of the treatment of a patient with STEMI is
based on “time is muscle.” Therefore, all
communities should create and maintain a
regional system of STEMI care that includes
assessment and continuous quality improve-
ment of EMS and hospital-based activities. A
12-lead ECG must be done by EMS personnel
at the site of first medical contact (FMC).
• Reperfusion therapy should be administered
to all eligible patients with STEMI with symp-
tom onset within 12 hours. Indications for
primary angioplasty and comparison with
fibrinolytic therapy are described in Table 2.
Primary PCI (Fig. E4) is the recommended
method of reperfusion when it can be per-
formed in a timely fashion by experienced
operators with an ideal FMC-to-device time
system goal of 90 minutes or less.
• In the absence of contraindications, fibrinolyt-
ic therapy (Table 3) should be administered to
patients with STEMI at non-PCI-capable hos-
pitals when the anticipated FMC-to-device
time at a PCI-capable hospital exceeds 120
minutes because of unavoidable delays. It
should be administered within 30 minutes of
hospital arrival.
• PCI is superior to thrombolytic therapy and is
the standard of care. It is effective and gener-
ally results in more favorable outcomes than
thrombolytic therapy.
• Primary PCI should be performed in patients
with STEMI and persistent ischemic symp-
toms and who have contraindications to fibri-
nolytic therapy, irrespective of the time delay
from FMC, or in patients with cardiogenic
shock or acute severe HF irrespective of time
delay from myocardial infarction (MI) onset.
Coronary stents (drug-eluting or bare-metal)
are useful in patients with STEMI.
• The question of culprit vessel vs. com-
plete revascularization during PCI has been
brought up since the stent technology was
applied to the management of STEMI. The
most recent clinical trials and observational
studies appear to favor complete revascular-
ization in the setting of STEMI, but the results
of larger ongoing trials are necessary to tip
the balance one way or the other in terms
of mortality and morbidity (contrast use,
radiation usage, length of the procedure) in
this situation. In the meantime, the approach
to each individual patient must be tailored
to the patient’s characteristics and social
circumstances.
 Myocardial Infarction 929

Triage: Patient with history suggestive of ACS

Duration of symptoms ≤12 hours
Vital signs
M
Immediate ECG reviewed by MD: STEMI

Prehospital notification PCI-capable PCI-capable

of STEMI facility? facility?

and Disorders
Diseases
Yes No

EP activates cath lab Transfer strategy Fibrinolytic

team with single page (DTB must be strategy
(if prenotification, activate
prior to patient arrival)
consistently ≤90 min) I
Arrange transfer to IV, oxygen, monitor
PCI-capable facility ASA 162-325 mg chewed
(clopidogrel if ASA-allergy)

IV, oxygen, travel monitor Contraindications to

ASA 162-325 mg chewed fibrinolytic therapy?
(clopidogrel if ASA-allergy)
Prepare patient for transfer to cath lab

No Yes

IV UFH (60 U/kg bolus (max 5000); Administer fibrinolytic Transfer to PCI-capable
12-15 U/kg/hr (max 1000 U/hr) agent within 30 min of facility or medical
* Note: hold β-blocker if (1) signs of door-time management as below
CHF or AV block, (2) age > 70 yr, (bolus agent preferred) unless contraindicated
(3) SBP <120 mm Hg or
(4) HR >100 bpm or < 60 bpm

*IV beta blocker if no contraindication

IV UFH: 60 U/kg bolus (max 4000);
Nitroglycerin if no contraindication
12 U/kg/hr (max 1000 U/hr)
• May substitute enoxaparin if age
*Consider GP 2b-3a inhibitor
*Consider clopidogrel 300-600 mg PO <75 and normal renal function
*Consider morphine * Note: hold β-blocker if (1) signs of
CHF or AV block, (2) age > 70 yr,
*Note: do not delay cath lab transfer (3) SBP <120 mm Hg or
for these medications (4) HR >100 bpm or < 60 bpm
*IV beta blocker if no contraindication
Clopidogrel 300 mg PO
Nitroglycerin if no contraindication
To cath lab Consider morphine

To CCU

FIG. 2  Assessment and treatment algorithm for ST-segment elevation myocardial infarction (STEMI).
ACS, Acute coronary syndrome; ASA, acetylsalicylic acid; AV, atrioventricular; bpm, beats per minute; cath lab,
catheterization laboratory; CCU, cardiac care unit; CHF, congestive heart failure; DTB, door-to-balloon time; ECG,
electrocardiogram; EP, emergency physician; GP, glycoprotein; HR, heart rate; IV, intravenous/intravenous line; PCI,
percutaneous coronary intervention; PO, orally; SBP, systolic blood pressure; UFH, unfractionated heparin. (From
Adams JG, et al.: Emergency medicine, clinical essentials, ed 2, Philadelphia, 2013, Elsevier.)

• 
For patients presenting to a non–PCI-
capable hospital, rapid assessment should
be done of (1) the time from onset of
symptoms, (2) the risk of complications
related to STEMI, (3) the risk of bleeding
with fibrinolysis, (4) the presence of shock
or severe HF, and (5) the time required for
transfer to a PCI-capable hospital and a
decision about administration of fibrinolytic
therapy reached. Because the effectiveness
of thrombolytics is time dependent, these
agents should ideally be administered either
in the field or within 30 min of the patient’s
arrival to the emergency department (door-
to-needle time).

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930 Myocardial Infarction

Triage: Patient with history suggestive of ACS

Vital signs
Immediate ECG reviewed by MD

ST depression ST-segment
ECG
or transient ST elevation, LBBB not
normal or
elevation not meeting known to be old, or
nondiagnostic
STEMI criteria acute posterior MI

Very low suspicion Clinical concern STEMI

of ACS for ACS pathway

Evaluate for other IV, oxygen, monitor

causes of symptoms Cardiac biomarkers
(troponin +/– others)
Repeat ECG for changes
in symptoms

ASA 162-325 mg PO chewed (clopidogrel if ASA-allergy)

Nitroglycerin (unless contraindicated)
IV beta blockers (unless contraindicated)
Enoxaparin (1 mg/kg) or UFH (weight-adjusted bolus/infusion)
Consider morphine

Troponin Troponin
negative positive

If high-risk
features or
Consider clopidogrel Cardiac consultation for catheterization within
second
Assess for high-risk clinical features 24-48 hrs unless contraindicated
troponin +
(persistent chest pain, ongoing/ Consider small molecule GP 2b-3a
worsening ST changes, VT, inhibitor (unless catheterization not planned)
age >75, CHF, hemodynamic Consider clopidogrel if CABG
instability) unlikely or catheterization not planned
Repeat biomarkers in 4-6 hrs if
still in ED

To CCU (or transfer

Admit to telemetry bed if catheterization not
available on site)

FIG. 3  Assessment and treatment algorithm for non–ST-segment elevation myocardial infarction.
ACS, Acute coronary syndrome; ASA, acetylsalicylic acid; CABG, coronary artery bypass grafting; CCU, cardiac
care unit; CHF, congestive heart failure; ED, emergency department; ECG, electrocardiogram; GP, glycoprotein;
IV, intravenous/intravenous line; LBBB, left bundle branch block; MI, myocardial infarction; STEMI, ST-segment
elevation myocardial infarction; UFH, unfractionated heparin; VT, ventricular tachycardia. (From Adams JG,
et al.: Emergency medicine, clinical essentials, ed 2, Philadelphia, 2013, Elsevier.)

• 
Fibrinolytic therapy: if tissue plasminogen
activator (t-PA) or reteplase is used, anti-
coagulants, such as heparin, are given to
increase the likelihood of patency in the
infarct-related artery for 48 hr and preferably
for the duration of the index hospitalization,
up to 8 days. In patients receiving fibrinolysis
for STEMI, treatment with enoxaparin is
superior to treatment with unfractionated
heparin for 48 hr but is associated with an
increase in major bleeding episodes. In
patients receiving streptokinase or APSAC,
heparin after thrombolysis is not indicated
because it does not offer any additional
benefit and can result in increased bleeding
complications. Tenecteplase and reteplase
are comparable with accelerated infusion
recombinant t-PA in terms of efficacy and
safety but are more convenient because
they are administered by bolus injection.
Lanoplase and heparin bolus plus infusion

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 Myocardial Infarction 931

• The use of mechanical circulatory support

TABLE 2  Indications for Primary Angioplasty and Comparison with
Fibrinolytic Therapy
is reasonable in patients with STEMI who
are hemodynamically unstable and require M
Indications urgent CABG.
• Until the catheterization team is ready or
Alternative recanalization strategy for ST segment elevation or LBBB acute MI within 12 hr of symptom onset
(or >12 hr if symptoms persist) fibrinolytics are administered, medical ther-
apy should be initiated immediately in the
Cardiogenic shock developing within 36 hr of ST segment elevation/Q wave acute MI or LBBB acute MI in
patients >75 yr old who can be revascularized within 18 hr of shock onset emergency department. This includes:
1. Routine measures
Recommended only at centers performing >200 PCI/yr with backup cardiac surgery and for operators perform-
ing <75 PCI/yr a. Oxygen: supplemental oxygen should
be administered to patients with arte-
Advantages of Primary PCI
rial oxygen desaturation (SaO2 less
Higher initial recanalization rates
than 90%). No benefit has been dem-

and Disorders
Diseases
Reduced risk of intracerebral hemorrhage onstrated to supplemental oxygen in
Less residual stenosis; less recurrent ischemia or infarction patients with normal SaO2.
Usefulness when fibrinolysis contraindicated b. Nitroglycerin: increase oxygen sup-
Improvement in outcomes with cardiogenic shock ply by reducing coronary vasospasm
Disadvantages of Primary PCI (Compared with Fibrinolytic Therapy) and decrease oxygen consumption by
Access, advantages restricted to high-volume centers, operators
Longer average time to treatment
reducing ventricular preload. Patients
with ongoing ischemic discomfort I
Greater dependence on operators for results should receive sublingual nitroglyc-
erin every 5 minutes for a total of 3
Higher system complexity, costs
doses, after which an assessment
LBBB, Left bundle branch block; MI, myocardial infarction; PCI, percutaneous coronary intervention (includes balloon angioplasty, should be made about the need for
stenting). intravenous nitroglycerin. Intravenous
From Goldman L, Schafer AI: Goldman’s Cecil medicine, ed 24, Philadelphia, 2012, Saunders. nitroglycerin is indicated for relief of
ongoing ischemic discomfort, control
of hypertension, or management of
TABLE 3  Dosing Regimens of Commonly Used Thrombolytic Agents pulmonary congestion. Nitrates should
not be administered to patients whose
Thrombolytic Agents Dosing Regimen systolic blood pressure is <90 mm
Hg or ≥30 mm Hg below baseline or
t-PA (alteplase) 15 mg bolus IV, followed by 0.75 mg/kg body weight (not to exceed 50 mg) severe bradycardia (<50 beats/min),
over 30 min, followed by 0.5 mg/kg (not to exceed 35 mg) over 60 min
tachycardia (>100 beats/min), or sus-
r-PA (reteplase) Two 10-U IV boluses, given 30 min apart pected RV infarction. Nitrates should
TNK–t-PA (tenecteplase) Single bolus IV 0.5 mg/kg (dose rounded to the nearest 5 mg, ranging from 30 not be administered to patients who
to 50 mg) have received a phosphodiesterase
Streptokinase 1.5 million U IV over 60 min inhibitor for erectile dysfunction with-
IV, Intravenous; PA, plasminogen activator; r-PA, reteplase plasminogen activator; TNK–t-PA, tenecteplase tissue plasminogen
in the last 24 hr (48 hr for tadalafil).
activator; U, units. c. Adequate analgesia: morphine sulfate
From Andreoli TE, et al.: Andreoli and Carpenter’s Cecil essentials of medicine, ed 8, Philadelphia, 2010, Saunders. 2 to 4 mg IV initially with increments
of 2 to 8 mg IV at 5- to 10-min inter-
are as effective as tPA with regard to mortal- transfer to a PCI-capable facility is advisable vals can be given for severe pain
ity rate, but the rate of intracranial hemor- without waiting for lytic results. unrelieved by nitroglycerin. Morphine
rhage is significantly higher. • Transfer to a PCI-capable hospital: immedi- can reduce the catecholamine surge
• Absolute contraindications to thrombolytic ate transfer for STEMI patients who develop caused by anxiety and pain, par-
therapy (Table 4) include history of intra- cardiogenic shock or acute severe HF, irre- ticularly in patients with anterior
cranial hemorrhage, known intracranial spective of the time delay from MI onset. myocardial infarctions, which in turn
malignant neoplasm or arteriovenous mal- Urgent transfer if the patient demonstrates can reduce heart rate and PCWP,
formation, ischemic stroke within 3 months evidence of failed reperfusion or reocclusion the increased cardiac workload and
(except acute ischemic stroke within 4.5 h), after fibrinolytic therapy. oxygen demand, leading to decreased
suspected aortic dissection, active bleeding • Coronary angiography should not be per- ischemia and pulmonary congestion.
or bleeding diathesis (except menses), sig- formed within the first 2 to 3 hours after Hypotension from morphine can be
nificant closed head or facial trauma within administration of fibrinolytic therapy. Coronary treated with careful IV hydration with
3 months, intracranial or intraspinal surgery artery bypass graft (CABG): urgent CABG is saline solution. If sinus bradycardia
within 2 months, or severe uncontrolled indicated in patients with STEMI and coronary accompanies hypotension, use atro-
hypertension (unresponsive to therapy). For anatomy not amenable to PCI who have ongo- pine (0.5-1.0 mg IV q5min prn to a
streptokinase, this applies to prior treatment ing or recurrent ischemia, cardiogenic shock, total dose of 2.5 mg). Respiratory
within 6 months. severe HF, or other high-risk features. CABG is depression caused by morphine can
• Relative contraindications: history of chronic recommended in patients with STEMI at time be reversed with naloxone 0.8 mg.
severe, poorly controlled hypertension, SBP of operative repair of mechanical defects. Morphine sulfate and nitroglycerine
>180 mm Hg, DBP >110 mm Hg, history of • Therapeutic hypothermia should be started should be avoided in patients with
prior ischemic stroke more than 3 months, as soon as possible in comatose patients RV involvement who usually present
dementia, known intracranial pathology, trau- with STEMI and out-of-hospital cardiac with bradycardia and hypotension.
matic or prolonged CPR (>10 minutes), major arrest caused by ventricular fibrillation (VF) Pain management in these cases
surgery <3 weeks, recent internal bleeding or pulseless ventricular tachycardia, includ- should be provided preferentially with
within 2 to 4 weeks, noncompressible vas- ing patients who undergo primary PCI. meperidine 25 to 50 mg intravenously
cular punctures, pregnancy, active peptic • Immediate angiography and PCI when indi- q 4h, in combination with phener-
ulcer, oral anticoagulant therapy. After the cated should be performed in resuscitated gan 12.5 mg to prevent nausea and/
administration of thrombolytics, immediate out-of-hospital patients. or vomiting. Blood pressure support
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932 Myocardial Infarction
TABLE 4  Contraindications to Thrombolytic Therapy in Acute Myocardial
Infarction
Absolute
Suspected aortic dissection
Active bleeding*
Any prior cerebral hemorrhage
Intracranial neoplasm
Cerebral aneurysm or arteriovenous malformation
Ischemic cerebrovascular accident within 3 mo
Relative
Bleeding diathesis, coagulopathy, or anticoagulant use
Major surgery within 3 wk
Puncture of a noncompressible vessel, internal bleeding, or head or major body trauma within previous 2 wk
Nonhemorrhagic stroke or gastrointestinal hemorrhage within 6 mo
Proliferative retinopathy
Active peptic ulcer disease
History of chronic, severe, poorly controlled hypertension
Severe uncontrolled hypertension on presentation (systolic blood pressure >180 mm Hg or diastolic blood pres-
sure >110 mm Hg)
Traumatic or prolonged (>10 min) cardiopulmonary resuscitation
Pregnancy
*Does not include menstrual bleeding.
From Andreoli TE, et al.: Andreoli and Carpenter’s Cecil essentials of medicine, ed 8, Philadelphia, 2010, Saunders.
with normal saline solution is of criti-  
cal importance to maintain adequate
hemodynamics until optimal revascu-
larization is accomplished.
d. Aspirin 162 to 325 mg PO should
be crushed and chewed to enhance
drug absorption and delivery. It should
be given as soon as possible and
continued indefinitely, at 81 mg daily.
Depending on the clinical and ECG
findings, if the patient is suspected to
have a coronary anatomy that needs
CABG rather than PCI, aspirin should
be continued. P2Y12 receptor antago-
nists should be avoided because they
increase the perioperative bleeding
risk; on-pump surgery should be
deferred for at least 24 hours after
clopidogrel and ticagrelor. Off-pump
surgery might be considered within 24
hours of clopidogrel or ticagrelor if the
benefits of revascularization outweigh
the risk of bleeding. However, if the
coronary artery disease is likely to
benefit from PCI alone, then a loading
dose of clopidogrel 600 mg or ticagre-
lor 180 mg PO should be given as early
as possible or prasugrel 60 mg as early
as possible and no later than 1 hour
after PCI. P2Y12 receptor antagonist
should be continued for at least 1 yr
after primary PCI with stent for STEMI.
  
Cangrelor is the newest direct-acting  
P2Y12 platelet receptor inhibitor. It has
a similar chemical structure to ATP, with
a half-life of 3 to 6 minutes. It is given IV
as a bolus plus 120 minutes of infusion
at the time of primary PCI in patients who
are naïve to P2Y12 receptor antagonists.
It was approved by the FDA in 2015 after
the CHAMPION PHOENIX trial. Clopidogrel
and prasugrel should be started after its
infusion is finished. The ticagrelor loading
dose can be given during the infusion.
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New DAPT guidelines call for discontinu-
ation of these drugs at 6 months post PCI
since it has been clearly demonstrated
in clinical trial that prolongation of DAPT
beyond this period of time does not
provide additional benefits in terms of
preventing MI and death, and it is actively
associated with an increased risk for
cardiac mortality secondary to bleeding
complications.
2. In patients receiving fibrinolytics only or
balloon angioplasty without stent, P2Y12
antagonists can be given for as little as
14 days.
3. Beta-adrenergic blocking agents should
generally be given to all patients who
do not exhibit evidence of shock. Beta-
blockers are useful to reduce myocardial
oxygen consumption and prevent tachyar-
rhythmias. Early IV beta blockage (in the
initial 24 hr) followed by institution of an
oral maintenance regimen is also effec-
tive in reducing recurrent infarction and
ischemia. Oral beta-blockers should be
initiated in the first 24 hr in patients with
STEMI who do not have any of the follow-
ing: signs of HF, evidence of a low-output
state, increased risk for cardiogenic shock,
or other contraindications for its use (bra-
dycardia, PR interval more than 0.24 sec-
onds, second- or third-degree heart block,
active asthma, or reactive airways disease).
They should be continued during and after
hospitalization for all patients with STEMI
and with no contraindications to their use
for at least 2 yr. Patients with initial con-
traindications to the use of beta-blockers
in the first 24 hr after STEMI should be
reevaluated to determine their subsequent
eligibility. It is reasonable to administer
intravenous beta-blockers at the time of
presentation to patients with STEMI and
no contraindications to their use who are
hypertensive or have ongoing ischemia.
4. Anticoagulation therapy: STEMI is due to
plaque rupture exposing the underlying col-
lagen platelets that are activated, and the
coagulation cascade is initiated. IV unfrac-
tionated heparin, bivalirudin, subcutaneous
enoxaparin, or fondaparinux can be used.
In patients at high risk of bleeding, use of
bivalirudin is reasonable. Anticoagulation
therapy is usually continued for 48 hours
after administration of lytic therapy unless
streptokinase or APSAC is used.
5. In patients with acute MI, treatment with
drug-eluting stents is associated with
decreased 2-yr mortality rates and a
reduction in the need for repeated revas-
cularization procedures compared with
treatment including bare-metal stents.
6. Gp IIb/IIIa inhibitors in the era of DAPT
therapy and primary PCI have failed to
show benefit with “upstream” treatment.
Abciximab might be useful in the presence
of large thrombus burden during primary
PCI. For patients receiving bivalirudin as the
primary anticoagulant, routine adjunctive
use of GP IIb/IIIa inhibitors is not recom-
mended but may be considered as adjunc-
tive or “bail-out” therapy in selected cases.
CHRONIC Rx
• Discharge medications in all patients with MI
(unless contraindicated) should include antiisch-
emic medications (e.g., nitroglycerin, beta-
blocker), lipid-lowering agents, and antiplatelet
therapy (aspirin and/or P2Y12 antagonists).
• Aspirin, 81 mg PO daily, but should be
continued indefinitely unless not tolerated
(e.g., GI bleed). Clopidogrel 75 mg PO daily;
ticagrelor, 90 mg bid, or prasugrel, 10 mg
PO daily, can be combined with aspirin and
should be continued without interruption for
a minimum of 30 days after bare-metal stent
placement or for 6 to 12 months after drug-
eluting stent placement; however, aspirin
should be continued indefinitely. Combining
P2Y12 antagonists with aspirin reduces risk
for repeat myocardial infarction and stent
thrombosis. If there is an elective surgical
intervention pending, it is recommended to
defer the surgery until completion of the full
course of the P2Y12 antagonist treatment.
• Angiotensin-converting enzyme inhibitors
(ACEIs) should be started within the first
24 hours of STEMI to all patients having
STEMI with anterior infarction, pulmonary
congestion, or LV EF <40%, in the absence
of hypotension. They reduce LV dysfunction
and dilation and slow the progression to
HF during and after acute MI. Angiotensin
receptor blockers (ARBs) should be given
to patients who have indication but are
intolerant of ACEIs. IV formulations of ACEIs
should not be given within the first 24 hours
of STEMI due to risk of hypotension. ARBs
offer no advantage over ACEIs and should be
considered only in patients who are intoler-
ant to ACEIs.
1. Commonly used ACEIs are ramipril 2.5 mg
PO bid, captopril 12.5 mg PO bid, enalapril
2.5 mg PO bid, and lisinopril 2.5-5 mg

PO qd initially, with subsequent titration
as needed. Ramipril is associated with a
lower mortality rate than most ACEIs.
2. ACEIs may be stopped in patients without
complications and no evidence of LV dys-
function after 6 to 8 weeks.
3.  ACEIs should be continued indefinitely
in patients with impaired LV function (EF
<40%) or clinical HF.
• Long-term aldosterone antagonist therapy
should be prescribed for post-STEMI patients
without significant renal dysfunction (cre-
atinine ≤2.5 mg/dl in men and ≤2.0 mg/dl
in women) or hyperkalemia who are already
taking an ACEI, a beta-blocker, and have LV
EF <40% with symptomatic HF or diabetes.
• High-dose statins should be started as early as
possible in all patients with STEMI regardless
of lipid panel, not only for their lipid-lowering
effects, but also their antiinflammatory proper-
ties (JUPITER trial), which can stabilize the rup-
tured plaque. Atorvastatin 80 mg can be used
(PROVE IT-TIMI 22 and MIRACL trials). A fasting
lipid panel should be checked during the first
24 hr of hospital course, and the intensive
therapy can be stepped down if appropriate.
Goal LDL cholesterol is <70 mg/dl.
COMPLICATIONS OF STEMI
Cardiogenic shock: emergent revascularization
with either PCI or CABG is the recommended
treatment.
Sustained ventricular tachycardia: implantable
cardioverter-defibrillator therapy (ICD) is indicated
before discharge in patients who develop sus-
tained ventricular tachycardia/ventricular fibril-
lation more than 48 hr after STEMI, provided the
arrhythmia is not due to transient or reversible
ischemia, reinfarction, or metabolic abnormalities.
Pacing in STEMI: temporary pacing is indicated
for symptomatic bradyarrhythmias unresponsive
to medical treatment and after revascularization.
AV block and bradyarrhythmias in the setting
of inferior wall MI are usually transient, will not
require long-term pacing, and usually resolve
within 2 to 4 weeks of the event. On the contrary,
AV block and bradyarrhythmias or new LBBB in
the presence of an anterior wall MI is usually a
sign of severe disruption of the bundle of His and
often requires a permanent pacemaker.
Pericarditis after STEMI: aspirin is recom-
mended for treatment of pericarditis after
STEMI. Glucocorticoids and nonsteroidal anti-
inflammatory drugs are potentially harmful for
treatment of pericarditis after STEMI.
EVALUATION OF POST-MI
PATIENTS
• Noninvasive testing for ischemia should be
performed before discharge to assess the
presence and extent of inducible ischemia
in patients with STEMI who have not had
coronary angiography and do not have high-
risk clinical features for which coronary
angiography would be warranted. It might be
considered before discharge to evaluate the
functional significance of a noninfarct artery
stenosis previously identified at angiography
and/or before discharge to guide the postdis-
charge exercise prescription.
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• Assessment of LV function: LV ejection frac-
tion should be measured in all patients with
STEMI. Echocardiography to rule out pres-
ence of mural thrombi in patients suspected
of having an extensive infarction (more com-
mon with anterior wall MI); contrast echo-
cardiography is added if mural thrombus is
suspected.
1.  Assessment of risk for sudden car-
diac death: Patients with an initially
reduced LV ejection fraction, <40%, who
are possible candidates for implant-
able cardioverter-defibrillator therapy
should undergo reevaluation of LV ejec-
tion fraction at 90 days (or 42 days if no
revascularization was performed). ICD
is recommended when LVEF remains
<35% in the presence of NYHA class II or
III heart failure, or in patients with LVEF
<30% regardless of symptoms, if the life
expectancy is >1 yr.
• Cardiac rehabilitation/secondary prevention
programs are recommended for patients with
STEMI.
• Lifestyle risk factors modification.
DISPOSITION
The prognosis after MI depends on multiple
factors:
• New bundle branch block, Mobitz II second-
degree block, and third-degree heart block
adversely affect outcome.
• Size of infarct: the larger it is, the higher the
post-MI mortality rate. Significant myocardial
stunning with subsequent improvement of
ventricular function occurs in most patients
after anterior MI. A lower level of creatine
kinase, an estimate of the extent of necrosis,
is independently predictive of recovery of
function.
• Site of infarct: inferior wall MI carries a
better prognosis than anterior wall MI; how-
ever, patients with inferior wall MI and right
ventricular involvement have a high risk for
arrhythmic complications and cardiogenic
shock.
• Ejection fraction after MI: the lower the LV
ejection fraction, the higher the mortality rate
after MI. The risk of death is higher in the
first 30 days after MI among patients with LV
dysfunction, HF, or both.
• Presence of post-MI angina indicates a high
mortality rate.
• Performance on low-level exercise test: the
presence of ST-segment changes during the
test is a predictor of high mortality rate dur-
ing the first year.
• Presence of pericarditis during the acute
phase of MI increases mortality rate at 1 yr.
• Type A behavior (competitive drive, ambi-
tiousness, hostility) is associated with a lower
mortality rate after symptomatic MI.
• The Killip classification is an independent
predictor of all-cause 30-day mortality:
1. Killip class I includes individuals with no
clinical signs of HF. Mortality rate is 6%.
2.  Killip class II includes individuals with
rales or crackles in the lungs, S3 gallop,
and elevated jugular venous pressure.
Mortality rate is 17%.
Myocardial Infarction 933
3. Killip class III describes individuals with
frank acute pulmonary edema. Mortality
rate is 38%. M
4.  Killip class IV describes individuals in
cardiogenic shock or hypotension (mea-
sured as systolic blood pressure <90 mm
Hg) and evidence of peripheral vasocon-
striction (oliguria, cyanosis, or sweating).
Mortality rate is 67%.
• Self-reported moderate alcohol consumption
in the year before acute MI is associated with
reduced 1-yr mortality rate.
• Discharge medication in patients with MI should
and Disorders
Diseases
include lipid-lowering agents. Statins may also
lower vascular inflammation and damage by
mechanisms other than reduction of low-den-
sity lipoprotein cholesterol. Early initiation of
statin treatment in patients with acute MI is
associated with reduced 1-yr mortality rate.
• Additional poor prognostic factors include ciga- I
rette smoking, history of hypertension or prior
MI, presence of ST-segment depression in acute
MI, older age, diabetes mellitus, and female sex
(especially women >50 yr). Lammintausta and
Fonarow reported that single men and women
who live alone have a 60% to 70% greater
risk of a heart attack. Furthermore, the study
showed >160% increase in the risk of sud-
den death in these groups when compared to
people who are married or live with family.
• Renal disease, even mild, as assessed by
the estimated glomerular filtration rate, is a
major risk factor for cardiovascular compli-
cations after MI.
• Although black patients with MI have worse
outcomes than their white counterparts,
these differences did not persist after adjust-
ment for patient factors and site of care.
PEARLS &
CONSIDERATIONS
COMMENTS
• Approximately 1.5 million patients undergo
PCI in the United States each year. Depending
on local practices and the diagnostic criteria
used, 5% to 30% of these patients have evi-
dence of a periprocedural MI.
• The 12-lead ECG has low sensitivity for the
detection of MI if the culprit lesion is in the left
circumflex artery (LCX). If the initial 12-lead
ECG is not diagnostic and high clinical suspi-
cion for acute coronary syndrome exists, it is
reasonable to obtain additional posterior chest
leads (V7 to V9) to detect LCX occlusion.
SUGGESTED READINGS
Available at ExpertConsult.com
RELATED CONTENT
Heart Attack (Patient Information)
Acute Coronary Syndrome (Related Key Topic)
Angina Pectoris (Related Key Topic)
Coronary Artery Disease (Related Key Topic)
AUTHORS: CLAUDIA SERRANO, M.D., and
JUAN A. ESCARFULLER, M.D.
Myocardial Infarction 933.e1

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